AR-C118925XX

• CAT Number: I002700
• CAS Number: 216657-60-2
• Molecular Formula: C28H23N7O3S
• Molecular Weight: 537.598
• Purity: ≥95%
• Target: P2Y2 receptor
• Solubility: Soluble in DMSO
• Storage: 0 - 4°Cfor short term (days to weeks), or -20 °C for long term (months).
• IUPAC Name: 5-[[5-(3,8-dimethyl-11H-dibenzo[1,2-a:1/',2/'-e][7]annulen-11-yl)-2-oxo-4-sulfanylidenepyrimidin-1-yl]methyl]-N-(2H-tetrazol-5-yl)furan-2-carboxamide
• InChI: InChI=1S/C28H23N7O3S/c1-15-3-8-20-17(11-15)5-6-18-12-16(2)4-9-21(18)24(20)22-14-35(28(37)30-26(22)39)13-19-7-10-23(38-19)25(36)29-27-31-33-34-32-27/h3-12,14,24H,13H2,1-2H3,(H,30,37,39)(H2,29,31,32,33,34,36)
• InChIKey: PVKNPGQAFNALOI-UHFFFAOYSA-N
• SMILES: CC1=CC2=C(C=C1)C(C3=C(C=C2)C=C(C=C3)C)C4=CN(C(=O)NC4=S)CC5=CC=C(O5)C(=O)NC6=NNN=N6

AR-C118925XX (CAT: I002700) is a selective antagonist of the P2Y2 receptor. P2Y2 receptors are a subtype of purinergic receptors that are involved in cellular signaling processes. By selectively blocking the P2Y2 receptor, AR-C118925XX inhibits the binding of specific extracellular signaling molecules, such as adenosine triphosphate (ATP) and uridine triphosphate (UTP), to the receptor. This antagonist action can modulate various cellular responses mediated by the P2Y2 receptor, such as calcium mobilization, ion channel activation, and release of inflammatory mediators. The selective inhibition of the P2Y2 receptor by AR-C118925XX provides a tool for studying the functional roles of this receptor and its involvement in various physiological and pathological processes.

Reference

1. Am J Respir Cell Mol Biol. 2004 Oct;31(4):446-55. Epub 2004 Jul 1.

Nucleotide-mediated mucin secretion from differentiated human bronchial
epithelial cells.

Kemp PA(1), Sugar RA, Jackson AD.

Author information:
(1)Novartis Respiratory Research Centre, Wimblehurst Road, Horsham, West Sussex
RH12 5AB, UK.

Most current cell-based models for examining the regulation of mucin secretion
demonstrate low signal-to-noise ratios, making experimental manipulation and data
interpretation difficult. Using adenosine triphosphate (ATP) as a mucin
secretagogue, we have developed a model of agonist-induced mucin secretion in
differentiated human bronchial epithelial cells. Mucin secretory signals were
estimated using enzyme-linked lectin assay, and typical signals of 300-400% of
baseline were observed in response to a 30-min exposure to ATP (100 microM). ATP
and uridine triphosphate equipotently stimulated mucin secretion consistent with
mediation via P2Y2 receptor activation. Suramin and AR-C118925XX, a competitive
P2Y2 receptor antagonist, inhibited adenosine 5/’-o-(3-thiotriphosphate)
(ATP-gammaS)-induced mucin secretion. A selective Gq G-protein antagonist
(GP-ANT)-2A completely abrogated ATP-gammaS-induced mucin secretion. Pertussis
toxin and the G(i/o)-specific, GP-ANT-2, had no effect. The phospholipase C
inhibitor, D609, and the protein kinase C inhibitor, calphostin C, substantially
inhibited ATP-gammaS-induced mucin secretion. Phorbol myristate acetate also
stimulated mucin secretion in a calphostin C-sensitive manner. ATP-gammaS-induced
mucin secretion was inhibited by the Ca2+ chelator, 1,2-bis(o-aminophenoxy)
ethane-N,N,N/’,N/’-tetra-acetic acid tetra (acetoxymethyl) ester. Ionomycin and
thapsigargin both stimulated mucin secretion. Our data are broadly consistent
with known G-protein-coupling and downstream signaling events associated with the
P2Y2 receptor. The exceptional signal-to-noise ratios obtained using this model
have permitted clear evaluation of the involvement of these mechanisms in
agonist-induced mucin secretion from differentiated human bronchial epithelial
cells.